Abstract
Hepatitis is a condition that can be self-limiting or can progress to fibrosis (scarring), cirrhosis, or liver cancer. These days, gut microbiota becomes an important part of our immune system, which is important for disease progression or recovery. Translocation of gut microbial and metabolic products causes intestinal inflammation by modulating immune cells leading to impairment of the primary barrier. But there are limited studies discussing pathogenesis and management of hepatitis with gut microbiota. In this review, we have discussed the role of gut microbiota in pathogenesis and management of various hepatitis, especially hepatitis B and C. We have discussed the role of bacterial products, LPS-TLR4 pathway, and unmethylated CpG DNA, which ultimately affects downstream NF-kB signaling in hepatitis. Finally, we have discussed the role of fecal microbiota transplantation in the management of hepatitis.
Highlights
Hepatitis is generally known as an inflammation of the liver that can be caused by hepatic and non-hepatic viruses, can be caused by alcohol, can be drug induced, and can be caused by autoimmunity
Gut microbiota composition is known to be associated with disease pathogenesis
Hepatitis C virus (HCV) caused 399,000 deaths with an estimated 71 million diagnosed with chronic infection in 2016. Both these viruses cause chronic infections at 10% in hepatitis B virus (HBV) and more than 30% in hepatitis C virus (HCV) leading to cirrhosis and hepatocellular carcinoma
Summary
Hepatitis is generally known as an inflammation of the liver that can be caused by hepatic and non-hepatic viruses, can be caused by alcohol, can be drug induced, and can be caused by autoimmunity. It increases the production of bile acids, which is important for gut microbiota (Ponziani et al, 2018) Some pathogenic bacteria such as Enterobacteriaceae, Staphylococcus, and Enterococcus decreased the bile acid in HCV-infected cirrhotic patients, which normalized after a direct-acting antiviral treatment. Kupffer cells as specialized macrophages are induced by the LPS-TLR4 pathway for the release of immunosuppressive mediators, such as IL-10, which in turn suppress the release of inflammatory mediators by Kupffer cells (Dixon et al, 2013) In this way, during viral hepatitis, virus specific immune responses are suppressed and inhibit efficient clearing of bacteria as well as viruses. These downstream pathways help in the activation of DCs for the secretion of cytokines and Frontiers in Cellular and Infection Microbiology | www.frontiersin.org
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